No Evidence That Genetic Variation in the Myeloid-Derived Suppressor Cell Pathway Influences Ovarian Cancer Survival

Sucheston-Campbell LE, Cannioto R, Clay AI, Etter JL, Eng KH, Liu S, Battaglia S, Hu Q, Szender JB, Minlikeeva A, Joseph JM, Mayor P, Abrams SI, Segal BH, Wallace PK, Soh KT, Zsiros E, Anton-Culver H, Bandera EV, Beckmann M, Berchuck A, Bjorge L, Bruegl A, Campbell IG, Campbell SP, Chenevix-Trench G, Cramer DW, Dansonka-Mieszkowska A, Dao F, Diergaarde B, Doerk T, Doherty JA, Du Bois A, Eccles D, Engelholm SA, Fasching P, Gayther SA, Gentry-Maharaj A, Glasspool RM, Goodman MT, Gronwald J, Harter P, Hein A, Heitz F, Hillemmanns P, Hogdall C, Hogdall EVS, Huzarski T, Jensen A, Johnatty SE, Jung A, Karlan BY, Klapdor R, Kluz T, Konopka B, Kjaer SK, Kupryjanczyk J, Lambrechts D, Lester J, Lubinski J, Levine DA, Lundvall L, Mcguire V, Mcneish IA, Menon U, Modugno F, Ness RB, Orsulic S, Paul J, Pearce CL, Pejovic T, Pharoah P, Ramus SJ, Rothstein J, Rossing MA, Rübner M, Schildkraut JM, Schmalfeldt B, Schwaab I, Siddiqui N, Sieh W, Sobiczewski P, Song H, Terry KL, Van Nieuwenhuysen E, Vanderstichele A, Vergote I, Walsh CS, Webb PM, Wentzensen N, Whittemore AS, Wu AH, Ziogas A, Odunsi K, Chang-Claude J, Goode EL, Moysich KB (2017)


Publication Type: Journal article

Publication year: 2017

Journal

Book Volume: 26

Pages Range: 420-424

Journal Issue: 3

DOI: 10.1158/1055-9965.EPI-16-0631

Abstract

Background: The precise mechanism by which the immune system is adversely affected in cancer patients remains poorly understood, but the accumulation of immunosuppressive/protumorigenic myeloid-derived suppressor cells (MDSCs) is thought to be a prominent mechanism contributing to immunologic tolerance of malignant cells in epithelial ovarian cancer (EOC). To this end, we hypothesized genetic variation in MDSC pathway genes would be associated with survival after EOC diagnoses.Methods: We measured the hazard of death due to EOC within 10 years of diagnosis, overall and by invasive subtype, attributable to SNPs in 24 genes relevant in the MDSC pathway in 10,751 women diagnosed with invasive EOC. Versatile Gene-based Association Study and the admixture likelihood method were used to test gene and pathway associations with survival.Results: We did not identify individual SNPs that were significantly associated with survival after correction for multiple testing (P < 3.5 × 10-5), nor did we identify significant associations between the MDSC pathway overall, or the 24 individual genes and EOC survival.Conclusions: In this well-powered analysis, we observed no evidence that inherited variations in MDSC-associated SNPs, individual genes, or the collective genetic pathway contributed to EOC survival outcomes.Impact: Common inherited variation in genes relevant to MDSCs was not associated with survival in women diagnosed with invasive EOC. Cancer Epidemiol Biomarkers Prev; 26(3); 420-4. ©2016 AACR.

Authors with CRIS profile

Involved external institutions

Roswell Park Cancer Institute US United States (USA) (US) Ohio State University US United States (USA) (US) Kliniken Essen-Mitte DE Germany (DE) Danish Cancer Society Research Center DK Denmark (DK) Pomeranian Medical University / Pomorski Uniwersytet Medyczny w Szczecinie (PMU) PL Poland (PL) Maria Skłodowska-Curie Institute of Oncology / Centrum Onkologii–Instytut im. Marii Skłodowskiej-Curie w Warszawie PL Poland (PL) National Cancer Institute (NCI) US United States (USA) (US) Rutgers Cancer Institute of New Jersey US United States (USA) (US) Universitätsklinikum Hamburg-Eppendorf (UKE) DE Germany (DE) Duke University Medical Center US United States (USA) (US) University College London (UCL) GB United Kingdom (GB) Cedars-Sinai Medical Center US United States (USA) (US) Medizinische Hochschule Hannover (MHH) / Hannover Medical School DE Germany (DE) Oregon Health and Science University (OSHU) US United States (USA) (US) Beatson West of Scotland Cancer Centre (BWSCC) GB United Kingdom (GB) Uniwersytet Rzeszowski PL Poland (PL) Dartmouth College US United States (USA) (US) Stanford University US United States (USA) (US) Glasgow Royal Infirmary (GRI) GB United Kingdom (GB) Deutsches Krebsforschungszentrum (DKFZ) DE Germany (DE) Brigham and Women's Hospital (BWH) US United States (USA) (US) The University of Melbourne AU Australia (AU) Mayo Clinic US United States (USA) (US) University Hospital Leuven (UZ) / Universitaire ziekenhuizen Leuven BE Belgium (BE) University of Copenhagen DK Denmark (DK) University of Pittsburgh US United States (USA) (US) Katholieke Universiteit Leuven (KUL) / Catholic University of Leuven BE Belgium (BE) University of Cambridge GB United Kingdom (GB) Fred Hutchinson Cancer Research Center CA Canada (CA) NYU Langone Medical Center US United States (USA) (US) QIMR Berghofer Medical Research Institute (früher: the Queensland Institute of Medical Research) AU Australia (AU) Haukeland University Hospital / Haukeland universitetssykehus NO Norway (NO) University of California Irvine US United States (USA) (US) University of Southern California (USC) US United States (USA) (US) University of Southampton GB United Kingdom (GB) University of Texas Health Science Center at Houston (UTHealth) US United States (USA) (US) University of Virginia (UVA) US United States (USA) (US) University of New South Wales (UNSW) AU Australia (AU) Icahn School of Medicine at Mount Sinai US United States (USA) (US) University of Michigan US United States (USA) (US) University of Glasgow GB United Kingdom (GB)

How to cite

APA:

Sucheston-Campbell, L.E., Cannioto, R., Clay, A.I., Etter, J.L., Eng, K.H., Liu, S.,... Moysich, K.B. (2017). No Evidence That Genetic Variation in the Myeloid-Derived Suppressor Cell Pathway Influences Ovarian Cancer Survival. Cancer Epidemiology Biomarkers & Prevention, 26(3), 420-424. https://dx.doi.org/10.1158/1055-9965.EPI-16-0631

MLA:

Sucheston-Campbell, Lara E., et al. "No Evidence That Genetic Variation in the Myeloid-Derived Suppressor Cell Pathway Influences Ovarian Cancer Survival." Cancer Epidemiology Biomarkers & Prevention 26.3 (2017): 420-424.

BibTeX: Download